Heavy Metals and Membrane Functions of an Alveolar Epithelium
The anuran lung can be mounted as a planar sheet for assessment of bioelectric properties and solute and water permeation. The lung of the bullfrog exhibited a transmural electrical p.d. of 19 mV (pleura positive), a resistance of 700 ohm cm2 and a short-circuit current (Isc) of 27 μa/cm2. Isc reflected active Cl- secretion into the lumen by a transport mechanism located at the luminal border of the alveolar epithelial cell layer. Other halides and SCN- were secreted; other bathing solution ions and H2O followed the predictions for passive diffusion. Exposure of the luminal surface of the lung or disaggregated epithelial cells to heavy metals revealed two patterns of response. HgCl2 decreased Isc, cell ciliary motility and QO2; CdCl2 and NiCl2 inhibited only QO2 and cilia. Effects of CdCl2 were reversed by dimercaprol but not by albumin. SH agents limited but did not reverse HgCl2 toxicity. None of the metals altered osmotic flow across the lung even though most increased flow across the urinary bladder from the same species. The effects of HgCl2 on bioelectric properties reflected changes in ion permeation. HgCl2 followed by a SH compound stimulated Isc and the pleural to lumen Cl- flux selectively. Without complexer, transient stimulation was followed by a decrease in Isc and an indiscriminate increase in ion permeability. We conclude that responses to heavy metals separate functions of ciliated cells from Cl- transport by the non-ciliated epithelium. Furthermore, non-specific cell damage by HgCl2 can be limited by SH agents to a selective action on the Cl- pump.
KeywordsPermeability Toxicity Mercury DMSO Cobalt
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